PATHOGENETIC MECHANISMS OF HYPOXIC-ISCHEMIC BRAIN INJURY IN CHILDREN AFTER CLINICAL DEATH

Brain death in children after clinical death is one of the most complex and urgent problems of modern pediatric intensive care. Immaturity of the nervous system, high metabolic activity, functional instability of the blood–brain barrier, and incomplete myelination determine the increased vulnerability of the child’s brain to ischemia and hypoxia. This article reviews the main pathogenetic mechanisms: primary (global ischemia, energy deficit, ion imbalance, excitotoxicity), secondary (mitochondrial dysfunction, reperfusion injury, oxidative stress, blood–brain barrier disruption, neuroinflammation), as well as different forms of cell death (apoptosis, necrosis, pathological autophagy). Particular attention is paid to the morphological consequences for the developing brain, including white matter injury, delayed myelination, and loss of neuronal networks. In children, the transition from reversible to irreversible damage occurs faster than in adults, which significantly complicates prognosis and therapeutic interventions. Current understanding of the molecular and morphological mechanisms of brain death has practical significance for improving diagnostics, prognosis, and treatment in pediatric intensive care.